ArticleEye (London, England)2025
Long-term macular atrophy growth in neovascular age-related macular degeneration: influential factors and role of genetic variants.
Article in Eye (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Fluid Volumes Longitudinal Modeling to Predict Atrophy and Fibrosis in Neovascular Age-Related Macular Degeneration.Ophthalmology science · 2026Article
- The controversial role of nutraceuticals vs. drugs in proliferative retinopathies.Frontiers in neuroscience · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
objectivesThis retrospective cohort study aimed to assess the long-term growth and associated risk factors of macular atrophy (MA) in eyes with neovascular age-related macular degeneration (nAMD) treated with intravitreal anti-vascular endothelial growth factor (anti-VEGF) compounds.
methodsTwo hundred and six patients initiating anti-VEGF therapy were followed for 8 years using a treat-and-extend protocol. The study analysed correlations between MA growth (by square root transformation measured in infrared images) and clinical parameters, and genetic variants for AMD in the complement and lipid pathways and the ARMS2 gene.
resultsSeventy-six patients (n = 92 eyes) were included, with a mean age of 73.9 ± 7.9 years. Eyes received an average of 7.1 ± 3.2 anti-VEGF injections per year. The prevalence of MA increased from 28.3% at baseline to 78.3% at 8 years, exhibiting an average annual growth rate of 0.25 ± 0.22 mm. Correlations were found between MA growth and size, and number of atrophic foci at baseline, and the common ARMS2 variant. Eyes with subretinal fluid (SRF) at baseline showed less foveal atrophy at 8 years compared to those with IRF or both IRF and SRF. No correlation was observed between MA growth and genetic variants in the complement and lipid pathways.
conclusionMost eyes with nAMD under 8 years of anti-VEGF therapy developed MA, with significant growth. Correlations with baseline MA characteristics and the ARMS2 variant were identified. Further investigation is needed to understand the potential role of complement as a therapeutic target for preventing macular atrophy in nAMD-affected eyes.
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